Animals ; Female ; Pregnancy ; Pyrethrins ; toxicity ; Rats ; Rats, Wistar ; Teratogens ; toxicity

OBJECTIVETo study the teratogenicity of new high-energy compounds, 3, 4 two furazan-based oxidation furazan (DNTF) and the impact on human health, occupational exposure limits were provided for the following research.

METHODSPregnant SD rats were randomly divided into five groups by Standard teratogenicity test, including three dose groups (5.0, 15.8, 50.0 mg/kg), the negative control (vegetable oil), and the positive control group (CP 10.0 mg/kg). Each 10 to 15 rats were in one group. Gavage was consecutive for rats during pregnancy 7 ∼ 12 d and then sacrifice after 20 d.

RESULTSThere were no significantly difference between the three dose groups and negative controls in the pregnancy rate, the weight of pregnant rats, fetal weight, fetal growth, fetal malformation rate and internal organs,

CONCLUSIONThere were no maternal toxicity, embryo toxicity and teratogenicity for rats when DNTF in the range 5.0 ∼ 50.0 mg/kg.

Animals ; Female ; Nitrofurazone ; toxicity ; Pregnancy ; Rats ; Rats, Sprague-Dawley ; Teratogens

OBJECTIVETo detect the embryo toxicity and the teratogenicity of DNAN in rats and provide basic data to occupational protection.

METHODS120 adult female SD rats and 60 male rats are mating for 1: 1, and the pregnant rats were randomly divided into five groups by the pregnant time. The negative control group are gavaged with 4% starch, and the three experiment groups are gavaged with DNAN suspension with the dose of 5 mg/kg, 15 mg/kg and 45 mg/kg respectively, while the positive control give aspirin of 280 mg/kg. All rats of the five groups are administrated gavage from gestation day 5 (GD5) to GD19 continuously. The rats are dislocated in GD20, and the toxicity of embryo and toetus are detected.

RESULTSThe net weight growth in all three dose group are less than that of negative group, while the dead foetus in high dose group is more than negative group. Moreover, the body weight, body lenghth, tail lenghth and the anal genital distance of foetus rats in high dose group are all less than that of negative group. The foetus external malformations of three dose groups appear no significant compared with negative group.However, the prevalences of skeleton malformation in high dose group and the internal organs malformation in the median and high dose group appear significant higher than that of negative group. There are significantly maternal reproductive toxicity, embryo toxicity and toetus toxicity in positive group.

CONCLUSIONDNAN can induced maternal reproductive toxicity, embryo toxicity and the teratogenicity to rats.

Animals ; Anisoles ; toxicity ; Female ; Male ; Pregnancy ; Rats ; Rats, Sprague-Dawley ; Teratogens ; toxicity ; Toxicity Tests

OBJECTIVETo detect the toxicity and teratogenicity of 2, 2-dinitroethene-1, 1-diamine (FOX-7) in rats.

METHODS125 adult SD rats were randomly divided into five groups, which are negative control (0 mg/kg) , positive control (280 mg/kg aspirin) , and three dose groups (5, 15, and 45 mg/kg) . They were administrated by gavage once a day from the 5th days to 19th days after pregnancy. The weight changes and toxicity of pregnant rats are recorded within the study, and the skeleton and internal organs malformations are detected by the recommended methods.

RESULTSAfter 5 or 6 days being poisoned, the pregnant rats appear significantly toxicity symptoms, such as exciting, irritability, and so on. The net weight raise in high dose group is less than the negative group, while the numbers of dead foetus in median and high dose groups are both more than that of negative group. Comparing with the negative group, the body weight and body lenghth of foetus rats in median and high dose groups, and the tail lenghth in high dose group are lower significantly. There are no external malformations in negative group and three dose groups. However, the foetus of high dose group appear significant skeleton and internal organs malformation prevalences that are significant more than negative group, including lateral cerebral ventricles enlarged, which accounts for 9.17%, occipital bone lost, which accounts for 2.59%.

CONCLUSIONFOX-7 can induced maternal reproductive toxicity, foetus toxicity and teratogenicity hazards to rats.

Animals ; Body Weight ; Female ; Nitro Compounds ; toxicity ; Pregnancy ; Rats ; Rats, Sprague-Dawley ; Teratogens ; toxicity ; Toxicity Tests

The purpose of this study is to evaluate the embryotoxicity of alkaloids in Senecionis Scandentis Hebra on in vitro cultured mouse embryos. Mouse whole embryo culture (WEC) was applied in this study. Post-implantation (8.5 d) mouse embryos were isolated from their mothers, and cultured in medium of immediately centrifuged serum (ICS) with different concentrations of seneciphylline (target concentrations were 100, 50, 25 and 12.5 μg x mL(-1)) or senkirkine (target concentrations were 50, 25 and 12.5 μg x mL(-1)) for 48 h. After culturing completed, the development and organic morphodifferentiation of the cultured embryos were evaluated microscopically. Treatment with seneciphylline and senkirkine had adverse effects on the development and organic morphodifferentiation of embryos. The effect also had clear dose-response. Alkaloidals in Senecionis Scandentis Hebra had embryotoxicity on cultured embryos, which indicated that pregnant people exposed to Senecionis Scandentis Hebra may get potential risk on fetus.
Animals ; Embryo Culture Techniques ; Embryo, Mammalian ; drug effects ; Female ; Mice ; Pregnancy ; Pyrrolizidine Alkaloids ; toxicity ; Senecio ; chemistry ; Teratogens ; toxicity

Alkanes ; toxicity ; Animals ; Chromosome Aberrations ; Mice ; Mice, Inbred ICR ; Micronucleus Tests ; Mutagenicity Tests ; Mutagens ; Rats ; Rats, Sprague-Dawley ; Teratogens

OBJECTIVETo explore the sensitive point of embryotoxicity of carbon disulphide on female mice.

METHODSAt the phases of follicle developing, implanting and post-implantation of blastocyst, female mice were injected intraperitoneally with carbon disulphide 631.4 mg/kg per day for three days while controls with plant oil. All indexes were detected at the fourteenth day of pregnancy.

RESULTS(1) In follicle developing CS(2) exposed group, the weight of embryos fossa [(1.23 +/- 0.36) g was 41% less than that in controls [(2.08 +/- 0.48) g, P = 0.000], and in implanting CS(2) exposed group the weight of embryo fossa, and embryos [(1.27 +/- 0.97) g, and (0.12 +/- 0.09) g respectively] were 39% and 37% less than those in controls [(2.08 +/- 0.48), (0.19 +/- 0.06) g, P = 0.068, P = 0.045]; (2) In both follicle developing and implanting CS(2) exposed group, the weights of uterus and placenta were also less than those in controls (P < 0.01). (3) In post-implantation CS(2) exposed group, the above parameters were not significantly different from those in controls.

CONCLUSIONFollicle developing phase as well as implanting of blastocyst may be sensitive point for embryotoxicity induced by carbon disulphide.

Animals ; Carbon Disulfide ; toxicity ; Embryo Implantation ; drug effects ; Embryonic Development ; drug effects ; Female ; Male ; Mice ; Mice, Inbred Strains ; Pregnancy ; Teratogens ; toxicity

OBJECTIVETo explore the protective effect of modified danshou decoction (MDD) on teratogenicity of bisphenol A intoxicated pregnant rats.

METHODSForty-four successfully mated rats were randomly divided into 4 groups, 10 in the blank group and 10 in the model group, 12 in the MDD group and 12 in the positive control group. Bisphenol A (BPA) at the dose of 600 mg/kg was given to rats by gastrogavage in the latter three groups from the 1st day of mating to the 20th day, while the soybean oil was given to rats by gastrogavage in the blank group. No intervention was given to rats in the model group, but the normal saline, MDD condensed decoction, and shoutai pill (STP) condensed decoction was respectively given to rats in the rest three groups during the experimental period. All rats were sacrificed by the 20th pregnancy day.

RESULTSCompared with the model group, the body weight of pregnant rats and fetal rats, body length and tail length of the fetal rats significantly increased in the MDD group (P < 0.05). But the effect of MDD was superior to that of STP (P < 0.05). Moreover, the teratogenic rate was significantly lowered in the MDD group (P < 0.05).

CONCLUSIONMDD could promote the weight gaining of pregnant rats and fetal rats, improve the body length and tail length of fetal rats, and lower the teratogenic rate in fetal mice.

Animals ; Benzhydryl Compounds ; toxicity ; Drugs, Chinese Herbal ; pharmacology ; Female ; Phenols ; toxicity ; Pregnancy ; Rats ; Rats, Sprague-Dawley ; Reproduction ; drug effects ; Teratogens ; Weight Gain

The pharmaceutical ethynylestradiol (EE) is a potent endocrine modulator. Application enlargement of ethynylestradiol in clinics and abuse in livestock farming and fishing make it important to explore ethynylestradiol toxicological action on vertebrate embryonic development and to establish an in vivo method for EE toxicity detection efficiently and conveniently. In the present study, using a model animal zebrafish and 17alpha-ethynylestradiol as a representative compound, we have investigated EE2 teratogenicity, target tissues and target genes on zebrafish embryo. The results show that median teratogenesis concentration (TC50) of EE2 is 0.8 microg x mL(-1), and median lethal dose (LD50) is 3.3 microg x mL(-1). Targets of EE2 action were implicated in brain, eyes, heart, muscle, skeleton, pigment and viscera. Embryonic cardiac arrhythmia caused by EE2 is probably resulted from heart abnormal structure. The embryonic stage sensitive to EE2 mainly started at cleavage and last up to the organogenesis with time-accumulating effect. RT-PCR results indicate that EE2 treatment disturbed gene expression pattern at the early period of zebrafish embryonic development by suppressing transcription of gene boz that promotes brain development, upregulating genes for trunk and tail, such as ntl, spt, shh, and perturbing Nodal signal expression of TGFbeta superfamily, for example, cyc, sqt and oep. Using zebrafish, an efficient in vivo method for quick evaluation of EE toxicity on embryonic development has been developed.
Abnormalities, Drug-Induced ; etiology ; Animals ; Arrhythmias, Cardiac ; chemically induced ; embryology ; Dose-Response Relationship, Drug ; Embryo, Nonmammalian ; abnormalities ; drug effects ; Embryonic Development ; drug effects ; Ethinyl Estradiol ; administration & dosage ; toxicity ; Gene Expression Regulation, Developmental ; Teratogens ; toxicity ; Zebrafish ; abnormalities ; embryology

OBJECTIVETo explore the mechanism of cleft palate in mice induced by 2, 3, 7, 8-Tetrachlorodibenzo-p-dioxin (TCDD).

METHODSOn gestation day 10 (GD 10), 12 pregnant mice were randomly divided into two groups as the treated group and the control group with 6 mice in each group. The mice in the treated group received intragastric administration with 64 microg TCDD/kg, while the mice in the control group received equivalent corn oil. The embryos were examined under stereomicroscope to detect the incidence of cleft palate on GD 18.5. Another 18 pregnant mice were randomly divided into two groups (treated group and control group) on GD 10 with 9 pregnant mice in each group. Then each group was divided into 3 subgroups: GD 13.5, GD 14.5 and GD 15.5, with 3 pregnant mice in each subgroup. The palatal shelves were dissected from the embryos for RNA and DNA extraction on GD 13.5, GD 14.5 and GD 15.5. At last the expression of Smad 2-4 and Smad 7 mRNA was investigated by RT-PCR, and the TGF-beta3 promoter methylamine levels were investigated by methylation specific PCR (MSP).

RESULTSThe cleft palate mice model was established successfully by exposing pregnant C57BL/6J mice to TCDD. Total frequency of clefts was 100% in TCDD group, and the frequency of clefts was 0 in the control group. The relative expression of Smad 2 mRNA was 0.263 +/- 0.088, 0.296 +/- 0.016 and 0.159 +/- 0.027 in TCDD group, 0.180 +/- 0.042, 0.282 +/- 0.029 and 0.165 +/- 0.018 in control group. The relative expression of Smad 3 mRNA was 0.453 +/- 0.153, 0.551 +/- 0.160 and 0.328 +/- 0.049 in TCDD group, 0.375 +/- 0.126, 0.510 +/- 0.145 and 0.259 +/- 0.035 in control group. The relative expression of Smad 4 mRNA was 0.675 +/- 0.174, 0.577 +/- 0.070 and 0.396 +/- 0.066 in TCDD group, 0.557 +/- 0.138, 0.587 +/- 0.080 and 0.441 +/- 0.054 in control group. The relative expression of Smad 7 mRNA was 0.283 +/- 0.050, 0.320 +/- 0.068 and 0.169 +/- 0.045 in TCDD group, 0.207 +/- 0.043, 0.288 +/- 0.051 and 0.155 +/- 0.040 in control group. There was no significant difference between the TCDD treated mice and the control (P > 0.05). The TGF-beta3 promoters were at the un-methylation state both in the TCDD treated and control group.

CONCLUSIONIt suggests that TCDD could induce a stable formation of cleft palate, but it is not through the TGF-beta/Smad signaling nor through the modification of TGF-beta3 promoter methylation.

Animals ; Cleft Palate ; chemically induced ; DNA Methylation ; Female ; Mice ; Mice, Inbred C57BL ; Polychlorinated Dibenzodioxins ; toxicity ; Pregnancy ; Promoter Regions, Genetic ; Signal Transduction ; Smad Proteins ; metabolism ; Teratogens ; toxicity ; Transforming Growth Factor beta3 ; metabolism